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Background Angiostrongylus cantonensis  L5, parasitizing human cerebrospinal fluid, causes eosinophilic meningitis, which is attributed to tissue inflammatory responses caused primarily by the high percentage of eosinophils. Eosinophils are also involved in killing helminths, using the peroxidative oxidation and hydrogen peroxide (H 2 O 2 ) generated by dismutation of superoxide produced during respiratory burst. In contrast, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival. In previous study, we demonstrated the extracellular function of  Acan -Gal-1 in inducing the apoptosis of macrophages. Here, the intracellular functions of  Acan -Gal-1 were investigated, aiming to further reveal the mechanism involved in  A. cantonensis  L5 worms surviving inflammatory responses in the human central nervous system. Methods In this study, a model organism,  Caenorhabditis elegans , was used as a surrogate to investigate the intracellular functions of  Acan -Gal-1 in protecting the worm from its host’s immune attacks. First, structural characterization of  Acan -Gal-1 was analyzed using bioinformatics; second, qRT-PCR was used to monitor the stage specificity of  Acan-gal-1  expression in  A. cantonensis . Microinjections were performed to detect the tissue specificity of  lec-1  expression, the homolog of  Acan-gal-1  in  C. elegans . Third, microinjection was performed to develop  Acan-gal-1::rfp  transgenic worms. Then, oxidative stress assay and Oil Red O fat staining were used to determine the functions of  Acan -Gal-1 in  C. elegans . Results The results of detecting the stage specificity of  Acan-gal-1  expression showed that  Acan -Gal-1 was upregulated in both L5 and adult worms. Detection of the tissue specificity showed that the homolog of  Acan-gal-1  in  C. elegans ,  lec-1  was expressed ubiquitously and mainly localized in cuticle. Investigating the intracellular functions of  Acan -Gal-1 in the surrogate  C. elegans  showed that N2 worms expressing  pCe-lec-1::Acan-gal-1::rfp , with lipid deposition reduced, were significantly resistant to oxidative stress;  lec-1  mutant worms, where lipid deposition increased, showed susceptible to oxidative stress, and this phenotype could be rescued by expressing  pCe-lec-1::Acan-gal-1::rfp . Expressing  pCe-lec-1::Acan-gal-1::rfp  or  lec-1  RNAi in  fat-6;fat-7  double-mutant worms, where fat stores  were reduced, had no significant effect on the oxidative stress tolerance. Conclusion In  C. elegans  worms, upregulated  Acan- Gal-1 plays a defensive role against damage due to oxidative stress for worm survival by reducing fat deposition. This might indicate the mechanism by which  A. cantonensis  L5 worms, with upregulated  Acan- Gal-1, survive the immune attack of eosinophils in the human central nervous system. Graphical Abstract

Upregulated galectin-1 in Angiostrongylus cantonensis L5 reduces body fat and increases oxidative stress tolerance